Your SlideShare is downloading. ×
Pep ulcer
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×

Saving this for later?

Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime - even offline.

Text the download link to your phone

Standard text messaging rates apply

Pep ulcer

1,493
views

Published on

gen ppt about peptic ulcer

gen ppt about peptic ulcer

Published in: Health & Medicine

0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
1,493
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
108
Comments
0
Likes
1
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. PEPTIC ULCER DISEASE
  • 2. DEFINITION  The term 'peptic ulcer' generally refers to an ulcer or erosions in stomach or duodenum.  It may also occur in the jejunum after surgical anastomosis to the stomach (Gastrojejunostomy) or, rarely, in the ileum adjacent to a Meckel's diverticulum.
  • 3. Peptic Ulcer Disease
  • 4. Risk Factors  H.pylori infection : 90% of Peptic ulcer patients are infected with H.pylori.  NSAIDs  Stress  Others :  Infection : CMV, HSV  Drugs : Bisphosphonates, Chemotherapy, Clopidogrel, Crack cocaine, KCl Glucocorticoids, Mycophenolate Mofetil,  Misc : Basophilia in Myeloproliferative disease, Radiation therapy,Infiltrating disease, Sarcoidosis, Crohn’s disease.  Life time risk of developing Peptic ulcer is 10%
  • 5. Stomach Defense Systems  Mucous layer ◦ Coats and lines the stomach ◦ First line of defense  Bicarbonate ◦ Neutralizes acid  Prostaglandins ◦ Hormone-like substances that keep blood vessels dilated for good blood flow ◦ Thought to stimulate mucus and bicarbonate production
  • 6. H. Pylori HISTORY • 1874 : Bircher first described the organism • 1982 : Warren and Marshall confirmed Koch’s postulates named it“campylobacter pyloridis” • 1985 : Association with peptic ulcer • 1989 : Named as ‘helicobacter ‘(helico-curved)
  • 7. H. Pylori • H. pylori inf. is virtually always associated with chronic active gastritis. • But only 10–15% develop frank PUD. • Transmission not yet known. Most likely route is feco- oral. • H. pylori is able to fight off the acid with the enzyme urease. • Urease converts urea into bicarbonate and ammonia, which are strong bases. • These acid neutralizing chemicals around the H. pylori protect it from the acid in the stomach.
  • 8. General Peptic Ulcer Symptoms  Epigastric tenderness ◦ Gastric: Epigastrium; left of midline ◦ Duodenal: mid to right of Epigastrium  Sharp, burning, aching, gnawing pain  Dyspepsia (indigestion)  Nausea/vomiting  Belching
  • 9. Differentiating gastric from peptic ulcer disease  Duodenal ulcers - age 25-75 years.  Gastric ulcer - age 55-65 years  Pain awakening patient from sleep between 12-3 a.m. present in 2/3 duodenal ulcer patients and 1/3 gastric ulcer patients
  • 10. Complications of Peptic Ulcers  Hemorrhage ◦ Blood vessels damaged as ulcer erodes into the muscles of stomach or duodenal wall ◦ Coffee ground vomitus or occult blood in tarry stools  Perforation ◦ An ulcer can erode through the entire wall ◦ Bacteria and partially digested food spill into peritoneum=peritonitis  Narrowing and obstruction (pyloric) ◦ Swelling and scarring can cause obstruction of food leaving stomach=repeated vomiting
  • 11. HEMORRHAGE  Upper GI bleeding is the most common complication.  Sudden large bleeding can be life-threatening.  It occurs when the ulcer erodes one of the blood vessels, such as the gastro duodenal artery.  With massive bleeding the patient vomits bright red or coffee ground blood. Minimal bleeding from ulcers is manifested by occult blood in a tarry stool (malena).
  • 12.  Bleeding can occur as slow blood loss that leads to anemia or as severe blood loss that may require hospitalization or a blood transfusion.  Occurs in about 15% cases.  More common in Elderly (>60 yrs)
  • 13. OBSTRUCTION  Gastric outlet obstruction - scarring and swelling due to ulcers causes pyloric narrowing. Patient often presents with severe vomiting.  Peptic ulcers can also produce scar tissue that can obstruct passage of food through the digestive tract, causing pt to become full easily, to vomit and to lose weight.
  • 14. Clinical feature & management  Long history of DU  Persistent vomiting - Large & projectile - Contain previous food elements  Epigastric fullness, visible peristalsis and succussion splash  Dehydration & electrolyte disturbances  Metabolic alkalosis and tetany.  Wasting & malnutrition.
  • 15. Treatment  Correct fluid & electrolytes disturbance and improve nutrition  Treatment options include balloon dilation and stenting, but surgery with drainage procedure is usually required.
  • 16. PERFORATION  Perforation often leads to catastrophic consequences.  Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity.  Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain.  Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back.  Perforation in the CBD- aerobilia, cholangitis
  • 17. Perforated peptic ulcer  The first report of a series of patients presenting with perforation of a duodenal ulcer was made in 1817 by Travers.  The earliest operative description was made by Mikulicz in 1884 but the first successful operation for a perforated duodenal ulcer was not until 1894.
  • 18.  Helicobacter pylori is implicated in 70–92% of all Perforated Peptic Ulcers.  The second most common cause of perforated duodenal ulcer is the ingestion of NSAIDs.  The least common cause is pathologic hypersecretory states, such as Zollinger-Ellison syndrome, although these should be considered in all cases of recurrent ulcer after adequate treatment.
  • 19.  Overall incidence for admission with peptic ulceration is falling.  The number of perforated ulcers remains unchanged.  Sustained incidence possibly due to increased NSAIDs in elderly.  80% of perforated duodenal ulcers are H. pylori positive.  Men are much more affected than women.  Ratio is approximately 12 : 1 to 20 : 1.
  • 20. PATHOLOGY  Acute Perforation ◦ Stage of Peritonism  Acid peptic juice, bile and pancreatic juice come in contact with general peritoneal cavity.  Pt cries out in severe pain during this stage. ◦ Stage of Reaction  Peritoneum reacts to the chemical insult by secreting peritoneal fluid copiously(Sterile).  This gives relief to the pain and lasts for 3-6 hrs. ◦ Stage of Peritonitis  Acid secretion is abolished once perforation occurs.  Since there is no acid barrier, bacterial invasion becomes easy  There is diffuse bacterial peritonitis.
  • 21. DIAGNOSIS  The most characteristic symptom is the sudden onset of Epigastric pain.  The pain rapidly becomes generalized although occasionally it moves to the Rt Iliac Fossa (Through Paracolic gutters).  The patient stays still.
  • 22.  There may be a history of previous dyspepsia, previous or current treatment for a Peptic Ulcer, or ingestion of NSAIDs.  On examination the patient is in obvious pain.  The abdominal findings are characteristically described as of board-like rigidity.
  • 23.  With time the patient may improve with dilution of the duodenal contents by exudates from the peritoneum but this is later replaced by the signs and symptoms of bacterial peritonitis.  Once an ulcer perforates, the subsequent clinical picture is influenced by whether or not the ulcer self seals.
  • 24. INVESTIGATIONS  Plain x-rays of the abdomen with the patient in the upright position have been used in diagnosing perforated ulcer. Chest X-ray standing reveals free air under diaphragm.  Similarly, use of water-soluble contrast medium with an upper gastrointestinal tract series or computed tomography scan may increase the diagnostic yield.
  • 25. COMPLICATIONS  In most cases of perforation, gastric and duodenal content leaks into the peritoneum.  This content includes gastric and duodenal secretions, bile, ingested food, and swallowed bacteria.  The leakage results in peritonitis, with an increased risk of infection and abscess formation.  Subsequent collection of fluid in the peritoneal cavity due to perforation and peritonitis leads to inadequate circulatory volume, hypotension, and decreased urine output.
  • 26.  Abdominal distension as a result of peritonitis and subsequent ileus may interfere with diaphragmatic movement, impairing expansion of the lung bases.  Eventually, atelectasis develops, which may compromise oxygenation of the blood, particularly in patients with coexisting lung disease.  In more severe cases, shock may develop.
  • 27. Treatment Options  Principles of initial conservative treatment include nasogastric suction pain control antiulcer medication Antibiotics  Several surgical techniques have been employed in the treatment of perforated peptic ulcer. These include conservative surgery with patching of the ulcer, peritoneal lavage, and antiulcer medication. Definitive surgery with truncal vagotomy, highly selective vagotomy, or partial gastrectomy.
  • 28. Non surgical treatment  In 1935 Wangensteen noted that ulcers are able to self seal and reported on seven cases treated without surgery.  In 1946 this observation was confirmed by Taylor and he treated 28 cases without surgery with good success.  This was in the context of the high mortality and morbidity associated with surgical management at the time.
  • 29.  In 1989 a trial from Hong Kong by Crofts et al. showed that non-operative treatment for PPU was accompanied by a low mortality rate and was not associated with a large number of complications when the gastroduodenogram documented a sealed perforation .
  • 30. In a tertiary care GI centre,  When the diagnosis of a perforated duodenal ulcer is established the patient is aggressively resuscitated, nasogastric suction begun, and broad spectrum antibiotic cover instituted.  If a tension pneumoperitoneum embarrasses respiration this can be aspirated to release the pneumoperitoneum.  A gastroduodenogram is performed to confirm self- sealing.  The peritonitis should resolve in 4 to 6 hours and if there is continued major fluid loss after this time or if there are progressive signs of peritonitis or increasing pneumoperitoneum then surgical intervention is required
  • 31. Laparoscopic Surgery  The traditional management of a perforated duodenal ulcer has been a Graham Omental Patch and a thorough abdominal lavage.  More recently this has been shown to be able to performed using a laparoscope. The only proven advantage of the laparoscopic technique appears to be decreased postoperative pain.  Operating times are longer compared to open techniques and hospital time appears to be similar to conventional treatment.
  • 32. Definitive surgery  There is good evidence that, in the emergency situation, highly selective vagotomy (proximal gastric, or parietal cell vagotomy) combined with simple omental patch closure of the perforation, in patients without the risk factors mentioned above, is just as effective as that performed in the elective setting .  This is associated with a less than 1% mortality rate and a 4–11% ulcer recurrence rate. The success of this operation is surgeon-dependent.
  • 33.  There has been a return to the use of simple omental patch closure since the late 1970's with the introduction of post-operative H2 antagonists and more recently Proton Pump Blockers.  Over the last 10 years this trend has only grown stronger due to the discovery of the role of H. pylori in the pathogenesis of duodenal ulcer.
  • 34.  Given that H. pylori is able to be implicated in up to 90% of perforated duodenal ulcers it would seem logical to utilize patch closure and subsequent antibiotic treatment of the infectious agent saving definitive surgical ulcer management for those who fail this regimen.
  • 35. Anti H. pylori regimen  Omeprazole (Lanzoprazole) 20 mg BD  Clarithromycin 250 mg BD  Metronidazole 500 mg BD / Amoxycillin 1g BD OR  Omeprazole 20 mg BD  Bismuth Subsalicylate 2 tab QID  Metronidazole 250 mg QID  Tetracycline 500 mg QID
  • 36. THANK YOU